MECHANISMS OF VASCULAR INJURY AFTER SPINAL CORD TRAUMA

脊髓创伤后血管损伤的机制

• 批准号: 2269717
• 负责人: EDWARD L. HOGAN
• 金额: $ 18.1万
• 依托单位: MEDICAL UNIVERSITY OF SOUTH CAROLINA
• 依托单位国家: 美国
• 财政年份: 1994
• 资助国家: 美国
• 起止时间: 1994-08-01 至 1998-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2269717
• 关键词: blood vessels; cellular pathology; cytotoxicity; eicosanoid metabolism; inflammation; kinins; laboratory rat; neuroprotectants; nonhuman therapy evaluation; spinal cord injury; trauma

Early pharmacological intervention in acute spinal cord injury (SCI) is based on the premise that secondary injury following the initial insult contributes to ultimate spinal cord damage and neurologic deficit. This contention is strengthened by the recent observation of the Second National Acute Spinal Cord Injury Studies (NASCIS II) showing that high dose methylprednisolone given within 8 hours of injury improved neurologic recovery in patients with acute SCI. Progressive vascular injury after SCI contributes to secondary injury. Vascular injury is a prominent feature in acute inflammation. All the cardinal features of acute inflammation including deposition of acute inflammatory cells, accumulation of inflammatory mediators, endothelial damage leading to increased vascular permeability and edema formation have been noted in the injured cord. We will continue to explore the vascular mechanism of secondary injury focusing on post-traumatic inflammatory reaction in the pathogenesis of progressive vascular injury. The main theme of this proposal will be on the kininogen-kinin system and eicosanoid profile. The roles of cellular and humoral factors of inflammation relevant to kinin-eicosanoid cascade will be studied in depth to explore cellular and molecular mechanism of progressive vascular injury in the context of a post-traumatic inflammatory reaction. New therapeutic regimens will also be designed based on these studies.

急性脊髓损伤（SCI）的早期药物干预